Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 380, Issue 2, Pages 313-317Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2009.01.068
Keywords
Serum amyloid A; C-C chemokine motif ligand 2; Formyl peptide receptor like-1; Endothelial cells; Atherosclerosis
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Funding
- Dong-A University
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We investigated the effects of serum amyloid A (SAA) on the production of C-C chemokine motif ligand 2 (CCL2) and the mechanism underlying SAA action in human umbilical vein endothelial cells (HUVECs). Stimulation of HUVECs by SAA elicited CCL2 production in a concentration-dependent manner. SAA induced the activations of NF-kappa B and AP-1, which were essential for CCL2 production after SAA stimulation. HUVECs expressed formyl peptide receptor-like 1 (FPRL1), and short interfering RNA knockdown of FPRL1 nearly completely blocked SAA-induced CCL2 production in HUVECs. We suggest that SAA stimulates CCL2 production via FPRL1 and, thus, contributes to atherosclerosis. (c) 2009 Elsevier Inc. All rights reserved.
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